Identification of Key Genes and Pathways in Gefitinib-Resistant Lung Adenocarcinoma using Bioinformatics Analysis

Kailin Mao; Fang Lin; Yingai Zhang; Hailong Zhou

doi:10.1177/11769343211023767

Identification of Key Genes and Pathways in Gefitinib-Resistant Lung Adenocarcinoma using Bioinformatics Analysis

Evol Bioinform Online. 2021 Jun 11:17:11769343211023767. doi: 10.1177/11769343211023767. eCollection 2021.

Authors

Kailin Mao^{1

2}, Fang Lin³, Yingai Zhang^{2

4}, Hailong Zhou^{1

2

5}

Affiliations

¹ Key Laboratory of Topical Biological Resources of Ministry of Education, Hainan University, Haikou, China.
² School of Life Sciences, Hainan University, Haikou, China.
³ College of Ecology and Environment, Hainan University, Haikou, China.
⁴ Central Laboratory, Affiliated Haikou Hospital of Xiangya Medical College, Central South University, Haikou, China.
⁵ One Health Institute, Hainan University, Haikou, Hainan, China.

Abstract

Gefitinib resistance is a serious threat in the treatment of patients with non-small cell lung cancer (NSCLC). Elucidating the underlying mechanisms and developing effective therapies to overcome gefitinib resistance is urgently needed. The differentially expressed genes (DEGs) were screened from the gene expression profile GSE122005 between gefitinib-sensitive and resistant samples. GO and KEGG analyses were performed with DAVID. The protein-protein interaction (PPI) network was established to visualize DEGs and screen hub genes. The functional roles of CCL20 in lung adenocarcinoma (LUAD) were examined using gene set enrichment analysis (GSEA). Functional analysis revealed that the DEGs were mainly concentrated in inflammatory, cell chemotaxis, and PI3K signal regulation. Ten hub genes were identified based on the PPI network. The survival analysis of the hub genes showed that CCL20 had a significant effect on the prognosis of LUAD patients. GSEA analysis showed that CCL20 high expression group was mainly enriched in cytokine-related signaling pathways. In conclusion, our analysis suggests that changes in inflammation and cytokine-related signaling pathways are closely related to gefitinib resistance in patients with lung cancer. The CCL20 gene may promote the formation of gefitinib resistance, which may serve as a new biomarker for predicting gefitinib resistance in patients with lung cancer.

Keywords: Gefitinib-resistant; biomarker; microarray; non-small-cell lung cancer; protein–protein interaction.